2012 Fiscal Year Final Research Report
How does cystatin-C enhance CD4-independent HIV infection?
| Project/Area Number |
22590416
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Virology
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| Research Institution | Nagasaki University |
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Principal Investigator |
KUBO Yoshinao 長崎大学, 大学院・医歯薬学総合研究科, 准教授 (30273527)
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| Project Period (FY) |
2010 – 2012
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| Keywords | HIV / cystatin-C / カテプシンB / 自然免疫 |
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| Research Abstract |
HeLa cells were resistant to CD4-independent HIV infection. We identified cystatin-C (cathepsin protease inhibitor) that conferred HeLa cells susceptible to CD4-independent HIV infection. When target cells were treated with a low molecular weight cathepsin inhibitor, CA-074Me, CD4-independent HIV infection was enhanced. Because CD4-independent HIV infection was attenuated by an endocytosis inhibitor, the infection occurs through endosomes. When cathepsin activity is relatively higher, CD4-independent HIV infectivity may be reduced due to the degradation of HIV particlesincorporated into endosomes by cathepsin. Although murine leukemia virus (MLV) infection occurs via endosomes, MLV infection was rather suppressed by CA-074Me. This result indicates that cathepsin is required for MLV infection unlike CD4-independent HIV infection. Because MLV infection in XC cells is not suppressed by endosome acidificationinhibitors, it is widely accepted that MLV infection does not occur via endosomes specifically in XC cells. We found that MLV infection in XC cells occurs through endosomes, and cathepsin activated without endosome acidification in XC cells confers MLV infection resistant to endosome acidification inhibitors.
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Journal Title
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Journal Title
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Volume: 38
Pages: 861-9
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Author(s)
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